The increase in the production and storage of free fatty acids may be the mechanism by which angiotensin II relates with the development of insulin resistance. It has been demonstrated that the elevated levels of free fatty acids induce insulin resistance through the inhibition of the transport and phosphorylation of glucose at a muscular level, followed by a reduction of the glycogen synthesis and glucose oxidation. Additionally, it has been suggested that free fatty acids may interfere in the stimulation of insulin in the GLUT 4 and hexokinase activity. Also, angiotensin II has a stimulating effect on the transcription rate of the ob gene in human adipocytes. The ob gene is in charge of codifying the leptin protein, which inhibits the appetite and regulates the thermogenesis. The chronic and sustained increase in leptin levels leads to a leptin-resistance condition, a condition in which the hormone loses its physiological actions. The increase in the leptin levels produces a greater expression of UPC 2 (Uncoupling protein 2) in an action mediated by Peroxisome Proliferator-Activated Receptors (PPARs), which interferes with the mitochondrial respiration chain in the pancreatic beta cells, getting to a reduction in the ATP generation and blocking the first peak of insulin secretion. This offsetting mechanism seems to be opposed to the insulin's lipogenic effect and avoids greater lipid storage. Unfortunately, the derived consequences of this alteration in the insulin secretion are a lower efficacy to maintain the euglycemia and to maintain a glucidic homeostasis. On the other hand, the hyperleptinemia, by mediating the sympathetic activity and increasing the sodium renal resorption, leads to the increases of blood pressure, which adds to the greater expression of the angiotensinogen produced by hypertrophied lipid cells. These cells generate angiotensin II to activate the adipocyte differentiation and to regulate the fat storage in response to nutritional changes.